Lynn E. Dobrunz received her S.B. in Engineering and Applied Sciences from Harvard University in 1988. She was awarded a Ph.D. in Biomedical Engineering from The Johns Hopkins University School of Medicine in 1994. She did postdoctoral work with Charles F. Stevens in the Department of Molecular Neurobiology at The Salk Institute in La Jolla, CA, and joined the faculty of UAB in 1999. She is currently an Associate Professor of Neurobiology and an Associate Director of the UAB Comprehensive Neuroscience Center.

My labís research focuses on understanding the role of inhibitory interneurons in regulating synaptic plasticity and circuit function in hippocampus, both in normal brain and in rodent models of neuropsychiatric disorders. We currently have three major areas of investigation.
First, we are investigating the role of short-term plasticity in regulating the balance between excitation and inhibition in hippocampus. Alteration in the E/I balance is emerging as a general principle underlying a wide variety of disorders, including schizophrenia, bipolar disorder, depression, autism, Down Syndrome, and epilepsy. Short-term synaptic plasticity dynamically regulates both excitatory and inhibitory synapses, causing their strength to be rapidly modified depending on the pattern of input activity. However, relatively little is known about the overall effects of short-term plasticity on the E/I balance, and how this affects circuit function. We are investigating this in hippocampus, using a combination of electrophysiology and voltage-sensitive dye imaging in hippocampal brain slices.
In a second (related) project, we are investigating the effects of interneuron transcriptional dysregulation on hippocampal circuit function. Transcriptional dysregulation in inhibitory interneurons occurs in a variety of disorders, including schizophrenia, bipolar disorder, and epilepsy. In particular, a decrease in the calcium binding protein parvalbumin, which is found in an important subtype of GABAergic interneurons, is one of the most prevalent findings in postmortem tissue from schizophrenia patients. PGC-1α (peroxisome proliferator activated receptor  coactivator 1α) is a transcriptional co-activator in interneurons that regulates transcription of parvalbumin. Genetic deletion of PGC-1α in mice results in decreased protein expression of parvalbumin in interneurons, as well as decreases in several other synaptic proteins that have been shown to be reduced in postmortem tissue from schizophrenia patients. We are using PGC-1α-/- mice as a way to investigate the multi-factorial effects of interneuron transcriptional dysregulation on hippocampal synaptic and circuit function, using a combination of approaches including electrophysiology, voltage-sensitive dye imaging, optogenetics, pharmacology, and behavior. We are currently determining the effects transcriptional dysregulation on the dynamics of the E/I balance, on the regulation of hippocampal circuit function by dopamine, and on hippocampal dependent behavior.
In a third project, we are investigating the effects of Neuropeptide Y (NPY) on hippocampal circuit function and behavior. NPY is an endogenous neuropeptide with robust anxiolytic (anti-anxiety) properties that has been implicated in a wide variety of anxiety disorders, including posttraumatic stress disorder (PTSD). It is released by a subset of inhibitory interneurons that also release GABA. We are studying the mechanisms that regulate the firing of NPY interneurons in hippocampus, the release of NPY, and the effects of NPY on the E/I ratio and on hippocampal circuit function. We are also investigating the role of alterations in NPY release in a rodent model of stress-induced anxiety/PTSD, and testing the effects of manipulating NPY levels on anxiety and the susceptibility to PTSD-like symptoms.